Cleft palate is one of the most prevalent congenital malformations seen in man. Corticosteroid-induced cleft palate has been the object of extensive research; however the mechanism by which this birth defect is generated has not been established. The objectives of the research program deal with the possible mechanisms by which cortisone delays the movement of the palatal shelves, resulting in a decreased possibility for fusion. Because of the ease of detecting it and also because of its present or absent nature, this defect lends itself to many aspects of experimental teratogenesis. Palatal shelves from mouse embryos at day 14-18 gestation are isolated and the level of individual glycosaminoglycans measured at each gestational day. In the CD-1 embryo palatal fusion occurs between days 14 and 15. Following treatment of pregnant mice with cortisone, the glycosaminoglycan content is again measured and compared with that found in untreated controls.. The level of hyaluronidase in palatal tissue will be measured at each gestational day as will the effect of cortisone in glycosaminoglycan production by palatal shelves in culture.